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Cancer Epidemiology, Biomarkers & Prevention
Cancer Epidemiology, Biomarkers & Prevention

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Research Articles

Prospective Study of Genomic Hypomethylation of Leukocyte DNA and Colorectal Cancer Risk

Wen-Yi Huang, L. Joseph Su, Richard B. Hayes, Lee E. Moore, Hormuzd A. Katki, Sonja I. Berndt, Joel L. Weissfeld, Srinivasan Yegnasubramanian and Mark P. Purdue
Wen-Yi Huang
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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L. Joseph Su
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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Richard B. Hayes
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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Lee E. Moore
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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Hormuzd A. Katki
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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Sonja I. Berndt
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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Joel L. Weissfeld
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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Srinivasan Yegnasubramanian
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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Mark P. Purdue
Authors' Affiliations: Divisions of Cancer Epidemiology and Genetics and Cancer Control and Population Sciences, National Cancer Institute, NIH, Bethesda, Maryland; Division of Epidemiology, New York University School of Medicine, New York; Department of Epidemiology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania; and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
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DOI: 10.1158/1055-9965.EPI-12-0700-T Published November 2012
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Abstract

Background: Systematic genome-wide reductions of methylated cytosine (5-mC) levels have been observed in colorectal cancer tissue and are suspected to play a role in carcinogenesis, possibly as a consequence of inadequate folate intake. Reduced 5-mC levels in peripheral blood leukocytes have been associated with increased risk of colorectal cancer and adenoma in cross-sectional studies.

Methods: To minimize disease- and/or treatment-related effects, we studied leukocyte 5-mC levels in prospectively collected blood specimens of 370 cases and 493 controls who were cancer-free at blood collection from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Leukocyte 5-mC level was determined by a high-pressure liquid chromatography (HPLC)/tandem mass spectrometry method and expressed as the relative amount of methyl to total cytosine residues, or %5-mC. We estimated the association between colorectal cancer risk and %5-mC categories by computing ORs and 95% confidence intervals (CI) through logistic regression modeling.

Results: We observed no dose-dependent association between colorectal cancer and%5-mC categories (lowest vs. highest tertile: OR, 1.14; 95% CI, 0.80–1.63; Ptrend = 0.51). However, among subjects whose 5-mC levels were at the highest tertile, we observed an inverse association between natural folate intake and colorectal cancer (highest tertile of natural folate vs. lowest: OR, 0.35; 95% CI, 0.17–0.71; Ptrend = 0.003; Pinteraction = 0.003).

Conclusions: This prospective investigation show no clear association between leukocyte 5-mC level and subsequent colorectal cancer risk but a suggestive risk modification between 5-mC level and natural folate intake.

Impact: Adequate folate status may protect against colorectal carcinogenesis through mechanisms involving adequate DNA methylation in the genome. Cancer Epidemiol Biomarkers Prev; 21(11); 2014–21. ©2012 AACR.

Footnotes

  • Note: Supplementary data for this article are available at Cancer Epidemiology, Biomarkers & Prevention Online (http://cebp.aacrjournals.org/).

  • Received June 11, 2012.
  • Revision received August 31, 2012.
  • Accepted September 9, 2012.
  • ©2012 American Association for Cancer Research.
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Cancer Epidemiology Biomarkers & Prevention: 21 (11)
November 2012
Volume 21, Issue 11
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Prospective Study of Genomic Hypomethylation of Leukocyte DNA and Colorectal Cancer Risk
Wen-Yi Huang, L. Joseph Su, Richard B. Hayes, Lee E. Moore, Hormuzd A. Katki, Sonja I. Berndt, Joel L. Weissfeld, Srinivasan Yegnasubramanian and Mark P. Purdue
Cancer Epidemiol Biomarkers Prev November 1 2012 (21) (11) 2014-2021; DOI: 10.1158/1055-9965.EPI-12-0700-T

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Prospective Study of Genomic Hypomethylation of Leukocyte DNA and Colorectal Cancer Risk
Wen-Yi Huang, L. Joseph Su, Richard B. Hayes, Lee E. Moore, Hormuzd A. Katki, Sonja I. Berndt, Joel L. Weissfeld, Srinivasan Yegnasubramanian and Mark P. Purdue
Cancer Epidemiol Biomarkers Prev November 1 2012 (21) (11) 2014-2021; DOI: 10.1158/1055-9965.EPI-12-0700-T
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